(Press-News.org) A sugar-binding protein could fuel terrible inflammation and worsen sepsis, a disease that kills more than 270,000 people every year in the US alone, reports a team of researchers led by UConn Health in the 4 January issue of Nature Immunology.
Sepsis is caused mostly by bacterial infections. The immune system runs out of controls and triggers a cytokine storm, a condition in which inflammation-causing proteins flood the blood. Organs may break down, and death often follows.
Other diseases can also cause cytokine storms; medical historians believe cytokine storms were behind the lethality of the 1918-1919 flu epidemic, as well as the Black Death. Cytokine storms are also observed in patients with severe COVID-19 and believed to be involved in death in COVID-19.
A main trigger for the cytokine storms during sepsis is the overreaction of the body when it detects an infection inside the cells. When a cell detects bacteria or pieces of bacteria inside itself, it immediately activates enzymes that in turn activate a protein that pokes holes on the cell membrane from within, eventually causing the cell to burst open and spill cytokines into the bloodstream. Cytokines are alarm signals, calling in the immune system to fight the bacteria. Cytokines also make other cells more likely to burst open and sound the alarm. Usually, the system damps itself after a while and calms down, but in sepsis it spins out of control, causing more and more cells to burst and die and release even more cytokines into the bloodstream.
When cells burst open, they release not only cytokines, but also other danger molecules called alarmins that alarm the body of an infection or injury and can amplify the ongoing cytokine storm.
UConn Health immunologist Vijay Rathinam wanted to know which alarmins were released when a cell detected a specific kind of bacterial molecule called lipopolysaccharide inside itself. Dr. Ashley Russo, then a graduate student in the Rathinam lab, catalogued--in collaboration with immunologists Tony Vella and Antoine Menoret at UConn Health--proteins released by these cells when they detected lipopolysaccharide.
And they found something exciting. Galectin-1, a protein that binds sugars and sugar-coated proteins, seemed to be emanating from the cells. Interestingly, they found that galectin-1 is small enough to be slipping out of the holes poked in the cells' membrane, even before the cells burst open.
Once they noticed that, they began to look at the role galectin-1 played in sepsis. They found that galectin-1 seemed to be suppressing a brake on inflammation, causing the cytokine storm to ramp up. They also found that mice lacking galectin-1 had less inflammation, less organ damage, and survived longer than normal mice did during sepsis resulting from a bacterial infection and lipopolysaccharide.
To find out if galectin-1 is released during sepsis in human patients, the team collaborated with the Jena University Hospital's Drs. Deshmukh, Bauer, and Sponholz and found that sepsis patients had higher levels of galectin-1 than other non-sepsis patients in critical care and healthy people.
The team is considering whether galectin-1 might be a good drug target to help dampen cytokine storms during sepsis, as well as a useful marker doctors could use to identify critical ill patients at risk.
INFORMATION:
This study was made possible by key additional collaborations with the laboratories of Dr. Gabriel Rabinovich of the Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental, Consejo Nacional de Investigaciones Científicas y Técnicas in Buenos Aires, Argentina, Drs. Beiyan Zhou, Sivapriya Kailasan Vanaja, and Jianbin Ruan of UConn Health, and Dr. Greg Hudalla of University of Florida.
This project was funded by grants from the National Institutes of Health to Dr. Rathinam.
If you type into a search engine - "why do men have to wait before having sex again?" - you will very quickly come across Prolactin. This little hormone is thought to be involved in hundreds of physiological processes in the body. Among them is the male post-ejaculatory refractory period. This period begins when a male ejaculates and ends when he recovers his sexual capacity.
If you search a bit more, you'll see that this theory has even led to the development of so called "treatments". These promise to shorten the length of a person's refractory period by reducing their body's prolactin levels.
Well, here is some bad news for anyone who has bought any such merchandise. A new study in mice by scientists at the Champalimaud Centre for the Unknown ...
A research study at the University of Chicago has found that in pregnancy, while the T cell response to a fetus becomes tolerant to allow for successful pregnancy, the part of the immune system that produces antibodies (known as the humoral response) becomes sensitized, creating memory B cells that can later contribute to the rejection of a transplanted organ.
The results help to clarify why it is that the immune system can tolerate a fetus during pregnancy, but later may be more likely to become sensitized to and reject an organ transplant. The study was published on January 4, 2021 in the END ...
Polarons are fleeting distortions in a material's atomic lattice that form around a moving electron in a few trillionths of a second, then quickly disappear. As ephemeral as they are, they affect a material's behavior, and may even be the reason that solar cells made with lead hybrid perovskites achieve extraordinarily high efficiencies in the lab.
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By splitting energy conversion and emission processes between two molecules, the researchers achieved devices that produce pure-blue emission with high efficiency, maintain brightness for relatively long times, and lack any expensive metal atoms--a set of properties that has so far been difficult ...
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Now, a comprehensive analysis - led by Washington University School ...
New Columbia Engineering study--first to investigate the long-term effect of soil moisture-atmosphere feedbacks in drylands--finds that soil moisture exerts a negative feedback on surface water availability in drylands, offsetting some of the expected decline
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ANN ARBOR, Michigan -- Michael Green, M.D., Ph.D., noticed that when his patients had cancer that spread to the liver, they fared poorly - more so than when cancer spread to other parts of the body. Not only that, but transformative immunotherapy treatments had little impact for these patient.
Uncovering the reason and a possible solution, a new study, published in Nature Medicine, finds that tumors in the liver siphon off critical immune cells, rendering immunotherapy ineffective. But coupling immunotherapy with radiotherapy to the liver in mice restored the immune cell function and led to better outcomes.
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MADISON, Wis. -- Deforestation dropped by 18 percent in two years in African countries where organizations subscribed to receive warnings from a new service using satellites to detect decreases in forest cover in the tropics.
The carbon emissions avoided by reducing deforestation were worth between $149 million and $696 million, based on the ability of lower emissions to reduce the detrimental economic consequences of climate change.
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But getting to those new uses typically involves a mix of serendipity and time-consuming and expensive randomized clinical trials to ensure that a drug deemed effective for one disorder will be useful as a treatment for something else.
The Ohio State University researchers ...
The healing process that follows a brain injury could spur tumour growth when new cells generated to replace those lost to the injury are derailed by mutations, Toronto scientists have found. A brain injury can be anything from trauma to infection or stroke.
The findings were made by an interdisciplinary team of researchers from the University of Toronto, The Hospital for Sick Children (SickKids) and the Princess Margaret Cancer Centre who are also on the pan-Canadian Stand Up To Cancer Canada Dream Team that focuses on a common brain cancer known as glioblastoma.
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